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B Biswas

Publications and source records attributed to B Biswas.

At least 37 records · Page 2Linked to original sources

Hydroalcoholic human placental extract: skin pigmenting activity and gross chemical composition.

BACKGROUND: Vitiligo is a pigmentary disorder of the skin of unknown etiology. It is thought to be of autoimmune origin after demonstration of antibody-mediated destruction of melanocytes. Photochemotherapeutic PUVA therapy is widely used in vitiligo with about 33% success. Aqueous or hydroalcoholic extracts of human placenta of ill-defined composition have also been used therapeutically for vitiligo. A hydroalcoholic human placental extract has been developed by us with pigmenting activity based on experimental therapies. Its chemical analysis was the primary objective of this study. METHODS: For the guinea pig experiment, 20 drops of the extract or vehicle (60% alcohol) as control was topically applied around the nipples covering the areola zones of male immature white guinea pigs (wt. 175-250 g) daily for 60 days with 15 minutes infrared (IR) exposure used for vascular dilatation and enhancement of the absorption of the extract. Standard methods have been followed for all chemical analyses. RESULTS: The guinea pig experiment showed clear pigmentation and hypertrophy of the experimental nipples to varying degrees. Chemical analysis of the extract revealed the presence of small-molecular-weight proteins/peptides, lipids (including glycosphingolipids), carbohydrates, sialic acids, cholesterol, triglycerides, high density lipoproteins (HDL), and others, including amino acids, nucleotides, carotenes, vitamins, etc. CONCLUSION: Glycosphingolipids, known modulators of B and T cells, were reported capable of inducing adhesion, spreading, and motility of melanoma. It is present in the extract and, therefore, may lead to skin pigmentation through induction of melanocytes. Endothelin, a 21-amino acid peptide, detected in human placenta and possibly extractable by our process, has been reported to be indispensable for melanocyte growth.

Absorption↗

Pathogenic, immunologic, and molecular differences between two Ehrlichia risticii strains.

Ehrlichia risticii is the causative agent of Potomac horse fever (PHF), an acute infectious disease of horses. In the last few years, there have been several reports of PHF cases occurring even in vaccinated horses. We isolated a new strain of E. risticii (90-12 strain) from a vaccinated horse suffering from clinical PHF. The major pathogenic, immunologic, and molecular differences between the 90-12 strain and the 25-D stain, which was originally isolated during the outbreaks in 1984, were studied. The 90-12 strain was more pathogenic for mice and horses compared with the 25-D strain. In enzyme-linked immunosorbent assay and immunofluorescence assay with mouse and horse antisera of both the strains, two- to fourfold differences were observed between (immunoblot) with mouse and horse antisera and also with the recombinant clone-specific antibodies. Though several antigens were similar in both the strains, there were significant differences between them in the 110-, 85-, 70-, 51-, and 33-kDa antigens. The 85-kDa antigen was present only in the 90-12 strain but cross-reacted with a 50-kDa antigen of the 25-D strain. The 51-kDa antigens of both strains had different migration patterns, Southern blot hybridization of the genome from both the strains with DNA probes made from the 51-, 55-, and clones for both the strains, whereas the probe of the 85-kDa clone showed a completely different pattern. The 16S rRNA gene sequences from the two strains were identical. Neither strain replicated in gamma interferon-treated mouse peritoneal macrophages. In in vitro neutralization assay, sera from the 25-D strain-infected horse neutralized the homologous strain but did not neutralize the 90-12 strain, whereas sera from the 90-12 strain-infected horse neutralized both the strains. In mouse protection experiments, there was complete homologous protection. But in cross-protection, mice immunized with the 25-D strain were only partially protected against challenge with the 90-12 strain, whereas mice immunized with the 90-12 strain were completely protected against the 25-D strain challenge. These results clearly indicate that there are major differences between the 90-12 and 25-D strains which may have implications regarding the vaccine failure for PHF and the development of an efficient vaccine.

Animals↗

Properties of mitochondrial DNA polymerase in mitochondrial DNA synthesis in yeast.

Mitochondrial DNA polymerase from Saccharomyces cerevisiae, purified 3500 fold, was separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis into three polypeptides. The major 150 kDa polypeptide was probably the catalytic subunit of the mitochondrial (mt) DNA polymerase and the other two polypeptides could be either proteolytic cleavage products of the polymerase, other subunits of the enzyme or protein contaminants. The mtDNA polymerase preferred an A+T-rich DNA template and did not require any RNA primer for DNA synthesis, at least under in vitro reaction conditions. It showed higher processivity on a double-stranded linear DNA template than on a single-stranded circular DNA template, and was capable of synthesizing at least about 1200 nucleotide primer-extended products without any major pause on a double-stranded DNA template.

Base Sequence↗

Detection of Ehrlichia risticii from feces of infected horses by immunomagnetic separation and PCR.

Potomac horse fever, caused by Ehrlichia risticii, is an important disease of equines. The major features of the disease are fever, leukopenia, and diarrhea. The organism has been detected from the blood mononuclear cells of infected horses, but its presence in the feces has not been known. A method for immunomagnetic separation of E. risticii from the feces of infected horses was developed, and the separated organisms were detected by PCR. Coating immunomagnetic beads (Dynabeads) with a 1:5 dilution of rabbit anti-E. risticii serum and incubating the Dynabeads with fecal samples for 25 min at room temperature gave optimum results. E. risticii was detected from the feces during the course of diarrhea from two experimentally infected horses. In horse 1, watery diarrhea occurred from days 11 to 16 postinfection (p.i.), after which the feces became soft on day 17 p.i. and then returned to normal. The organisms were first detected from the feces on day 11 p.i., peaked on day 13 p.i., and then gradually decreased until day 16 p.i., after which they became undetectable. In horse 2, first, on day 12 p.i., there was soft feces which continued and progressed to diarrhea on day 17 p.i. The feces became normal after day 18 p.i. The organisms in the feces of this horse were first detected on day 12 p.i. and peaked on day 14 p.i., after which they declined until day 16 p.i. and then became undetectable. In both horses, the number of organisms in the mononuclear cells peaked on days 10 and 11 p.i., respectively, 3 days prior to the respective peaks in the feces. E. risticii was not detected from the plasma samples obtained from these horses. There was a drastic reduction in PCR amplification of E. risticii DNA for fecal samples stored frozen at -20 degrees C in comparison with those stored at 4 degrees C. The presence of the organism in the feces only during the soft- or diarrheal-feces phase supports the previous hypothesis that the diarrhea is caused by the organisms replicating in cells lining the intestines. This rapid simple method of detection of the organisms from the feces will be helpful in diagnostic and epidemiologic studies of Potomac horse fever.

Animals↗

Diagnostic application of polymerase chain reaction for detection of Ehrlichia risticii in equine monocytic ehrlichiosis (Potomac horse fever).

Genomic amplification by the polymerase chain reaction (PCR) was used to identify a unique genomic sequence of Ehrlichia risticii directly in DNA isolated from peripheral-blood buffy coat cells of E. risticii-infected horses (Potomac horse fever) and from infected cell cultures. A specific primer pair, selected from a cloned, species-specific, 1-kb DNA fragment of the E. risticii genome as a template, was used for the amplification of the target DNA of 247 bp. The optimal number of 40 PCR cycles, determined by analyzing an amplification profile obtained with a constant Taq polymerase concentration, was used to achieve maximum amplification of the E. risticii DNA segment. Efficient amplification of target DNA was achieved with specimens processed by either the phenol extraction or rapid lysis method. The specificity of the amplified DNA product was confirmed by the proper size (247 bp) and appropriate restriction enzyme cleavage pattern of the amplified target DNA, as well as by the specific hybridization signal obtained by using a PCR-amplified 185-bp internal DNA probe. A 10(5)- to 10(6)-fold amplification of target DNA, which allowed detection of E. risticii from as few as two to three infected cells in culture and from a very small volume of buffy coat cells from infected horses, was achieved. This PCR amplification procedure was found to be highly specific and sensitive for the detection of E. risticii for the study of Potomac horse fever.

Animals↗

What do hospices do? A survey of hospices in the United Kingdom and Republic of Ireland.

OBJECTIVE: To obtain baseline information about hospice clinical activity. DESIGN: Survey of hospices by postal questionnaire and telephone interview. SETTING: 98 Hospices in the United Kingdom and Republic of Ireland of 111 that had a named matron or senior nurse, including 17 funded by NHS and 81 independent units. PARTICIPANTS: Hospice matrons or nursing sisters in charge, to whom the questionnaire was addressed. RESULTS: Median age of hospices was 7 years, and those built during the past seven years had a median of 12 inpatient beds. All NHS hospices had some input from a medical consultant whereas 12 (15%) of independent units did not. 72 Hospices had home care teams and 12 of 20 of these randomly contacted by telephone provided 24 hour cover. The median number of whole time equivalent nurses was four, but 6 (30%) of teams did not include a doctor. Wide variations were found in discharge rates (range 1-76%) and throughput (1.7-31.8 patients/bed/year). In units with a full time consultant or medical director throughput was greater and more patients had palliative surgery and became organ donors than in units without (45/48 v 38/50 and 45/48 v 25/50, respectively). With the exception of pulmonary function tests and insertion of nasogastric tubes and indwelling epidural catheters, tests and procedures were used by over 90% of hospices, although sometimes the patient had to be transferred elsewhere. CONCLUSIONS: Respondents from units with a full time consultant or medical director were more likely to choose a "technical" description of their unit, such as "a pain relief centre" than those without, who favoured non-technical descriptions. These differences are likely to increase with the appointment of more fully trained consultants in palliative medicine.

Home Care Services↗

Reversal of noradrenaline denervation-induced increase of beta-adrenoreceptor binding in rat neocortex by noradrenaline infusion.

The effect of intraventricular infusion of (-)-noradrenaline (NA) on beta-receptor binding in vitro to homogenates from 6-hydroxydopamine (6-OH-DA)-denervated and from normal rat cerebral cortex was studied. NA was infused with osmotic minipumps connected to cannulas placed in the right lateral ventricle, delivering 1 or 5 microgram (-)-NA/h continuously for 9 days. One day later the rats were sacrificed and cortical tissue taken for beta-receptor (using [3H]dihydroalprenolol ([3H]DHA) as radioligand) and NA assay. The NA level in the cerebral cortex of 6-OH-DA treated rats was decreased to 70-80% of that of controls. No substantial change in the NA level was observed after infusion of 1 microgram (-)-NA/h, whereas infusion of 5 microgram/h led to a 40-60% increase compared to that of control rats infused with vehicle alone. Infusion of vehicle alone into control rats did not cause any change in [3H]DHA binding, whereas in denervated rats there was a 30-50% increase in [3H]DHA binding compared to that of controls. This increase was completely counteracted by infusion of 1 or 5 microgram (-)-NA/h. Infusion of 1 microgram (-)-NA/h to control rats did not cause any change, while infusion of 5 microgram (-)NA/h led to a significant decrease (-24%) in [3]DHA binding. The present results further support the view that the availability of NA at the receptors controls the number of beta-adrenergic receptors, thereby probably regulating the NA sensitivity of cells with beta-receptors.

Animals↗

Effect of intraperitoneally administered GABA on the locomotor activity of mice.

Gammaaminobutyric acid (GABA) was injected intraperitoneally (i.p.) into mice at doses from 25--2000 mg/kg, and spontaneous locomotor activity was recorded for the following 20 min. A slight but significant decrease in the spontaneous locomotor activity was noted only with the highest dose. The stimulation of motor activity induced by ethanol (2.4 g/kg i.p.) was significantly counteracted by GABA (100 mg/kg i.p. and upwards). A further suppression of ethanol-induced hyperactivity was reached by pretreatment with aminooxyacetic acid (AOAA, 15 mg/kg i.p.). The stimulation of motor activity induced by morphine (10 mg/kg i.p.) remained unaffected by even high doses of i.p. GABA. Motility produced by activation of postsynaptic catecholamine receptors, i.e., by apomorphine (3 mg/kg i.p.) and clonidine (3 mg/kg i.p.) following reserpine (10 mg/kg i.p.) and alpha-methyltyrosine (250 mg/kg i.p.) pretreatment, was not affected by i.p. GABA injections, whereas hypomotility caused by a low dose of haloperidol (150 microgram/kg i.p.) was enhanced. In conjunction with earlier biochemical data, these results suggest a certain access of blood-borne GABA to the CNS, leading to inhibition of dopaminergic neurons involved in motility regulation.

Aminooxyacetic Acid↗

On the mode of action of diazepam on brain catecholamine metabolism.

Intraperitoneal injection of diazepam in moderate dosage (1--10mg/kg) to rats caused a decrease in dopa and 5-hydroxytryptophan (5-HTP) formation, measured as the accumulation of these intermediates induced by inhibition of the aromatic L-aminoacid decarboxylase by means of NSD 1015 (3-hydroxybenzylhydrazine (HCl), in limbic forebrain, striatum and the remaining hemisphere portion. These effects are opposite to those induced by gamma-aminobutyric acid (gaba) and gamma-butyrolactone (100 and 750 mg/kg i.p. respectively), and the effects of the latter agents were significantly counteracted by diazepam. The effect of diazepam on dopa formation persisted after the acute transection of dopaminergic axons (transverse cerebral hemisection at the level of the caudal hypothalamus). The elevation of dopamine following hemisection was also significantly counteracted on the hemisected side of the brain, the intact side remaining unchanged. The data do not support the hypothesis that benzodiazepines act by enhancing gabaergic transmission. They rather suggest that these agents exert an inhibitory action on transmitter synthesis and utilization at the synaptic level, i.e. an action not necessarily bearing any direct relationship to gaba.

4-Butyrolactone↗

Potentiation by neuroleptic agents of the inhibitory action of intraperitoneally administered GABA on the locomotor activity of mice.

The ability of several neuroleptics to potentiate the inhibitory action of IP administered GABA on the motor activity of mice has been investigated. Haloperidol, chlorpromazine, thioridazine, and clozapine, but not the apparently selective dopamine receptor-blocking agent spiperone, were found to possess such activity. Phenoxybenzamine also proved active in potentiating GABA. Thus blockade of dopamine receptors as well as alpha-adrenergic receptors may be responsible for neuroleptic-induced potentiation of GABA actions.

Animals↗

The effect of intracerebroventricularly administered GABA on brain monoamine metabolism.

Intracerebroventricular injection of gamma-aminobutyric acid (GABA) was performed in male rats and the brain monoamines, 5-hydroxyindoleacetic acid (5-HIAA), tyrosine and tryptophan levels were measured. GABA induced within 30 min a marked dose-dependent increase in the brain contents of dopamine (DA), serotonin (5-HT), tyrosine and tryptophan, while noradrenaline (NA) was lowered. Large doses of GABA, i.e. 1.5-3 mg/rat, were required for these effects. Aminooxyacetic acid (AOAA), an inhibitor of GABA-transaminase, when given alone in a dose of 25 mg/kg i.p. caused a significant rise of DA, 5-HT and tryptophan. The combination of GABA and AOAA raised these levels more than either agent alone. Picrotoxin (4 mg/kg, i.p.) a claimed GABA receptor antagonist partially counteracted the GABA-induced DA rise. Monoamine synthesis was studied in different parts of the brain by measuring the accumulated dopa and 5-hydroxytryptophan (5-HTP), 30 min after NSD 1015 (3-hydroxybenzylhydrazine HCl, 100 mg/kg) an inhibitor of aromatic L-amino-acid decarboxylase, given i.p. 5 min after GABA. GABA caused a marked rise in dopa formation both in DA- and NA-predominated brain regions. Also 5-HTP formation was enhanced. The effects on both dopa and 5-HTP formation showed marked regional differences. The data suggest that GABA, by activating specific receptors, causes inhibition of firing of dopaminergic neurones and the opposite effect on the noradrenergic neurones. The nature of the effect on 5-HT metabolism needs further investigation.

Aminobutyrates↗

The effect of intraperitoneally administered GABA on brain monoamine metabolism.

GABA was injected intraperitoneally to rats in single doses of 2.5 to 1500 mg/kg. Thirty minutes after injection a dose-dependent increase in dopamine (DA) and a decrease in noradrenaline (NA) content were observed in the brain. However, in the lowest dose range these levels showed small but significant changes in the opposite direction. The accumulation of dopa after inhibition of the aromatic L-aminoacid decarboxylase was enhanced by i.p. GABA both in DA- and in NA-predominated brain regions, the dose-response relations being complex. Increased levels of serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and tryptophan as well as enhanced accumulation of 5-hydroxytryptophan, induced by decarboxylase inhibition were also observed. The general pattern of effects was similar to that previously observed after intracerebroventricular injection of GABA, although the intraperitoneal doses required were higher. It is suggested that a certain penetration of GABA from the blood into the brain can occur, leading to changes in the physiological activity of monoaminergic neurons.

Aminobutyrates↗

Adrenocortical changes in rats during acute and chronic administration of delta-9-tetrahydrocannabinol.

Acute intraperitoneal administration of delta-9-THC (at doses of 10 mg/kg and 50 mg/kg) to adult male albino rats showed characteristic stimulating effect on adrenocortical tissues with marked depletion of ascorbic acid, cholesterol containing neutral lipids and significant increase in the delta5-3 beta -hydroxysteroid dehydrogenase and glucose-6-phosphate dehydrogenase activities in the zona fasciculata and zona reticularis regions. Adrenal weights and the histometric measurements of the adrenocortical areas showed no significant changes. Chronic intraperitoneal administration of delta-9-THC (at doses of 10 mg/kg per day for 15 days) produced marked accumulation of cholesterol containing neutral lipids, with increase in ascorbic acid and delta5-3 beta-hydroxysteroid dehydrogenase and glucose 6-phosphate dehydrogenase activities in the fasciculata-reticularis regions. Adrenal weights and histometric measurements revealed marked hypertrophy of the adrenal glands.

Adrenal Cortex↗